Sodium, survival, and the mechanical properties of the carotid artery in stroke-prone hypertensive rats.
BACKGROUND
Reduction in sodium intake improves the survival of stroke-prone spontaneously hypertensive rats (SHR-SP) without causing any change in their blood pressure.


OBJECTIVE
To investigate whether the diuretic indapamide improves survival of SHR-SP and whether changes in the structure and the function of large arteries are associated with survival.


METHODS
Forty-eight hypertensive rats aged 6 weeks were divided into three groups: a control SHR-SP group (n = 24) and a control spontaneously hypertensive rat (SHR) group (n = 12), with 1% saline drinking water; and an indapamide-treated SHR-SP group (n = 12) with 1% saline drinking water administered 1 mg/kg per day indapamide via their food. At the end of a 12-week follow-up period, pulsatile changes in blood pressure and common carotid artery diameter (measured by high-resolution echo-tracking techniques) were determined and aortic histomorphometry was performed.


RESULTS
By the end of the study 58% of the SHR-SP control group rats had died. There were no deaths in the other two groups. In these two groups the mean blood pressure (217+/-10 and 212+/-7 mmHg), carotid diameter and distensibility (0.48+/-0.09 and 0.61+/-0.22 mmHg[-1]), arterial thickness (116+/-4 and 116+/-3 microm), and collagen content of the arterial wall were identical. In the SHR-SP control group the mean blood pressure was significantly lower (168+/-9 mmHg), the carotid distensibility was higher (1.47+/-0.35 mmHg[-1]), and the arterial thickness (138+/-5 microm) and collagen content were substantially higher than those in the other two groups. In the study population as a whole, for a given mean arterial pressure the carotid distensibility was identical in the three groups, although the arterial thickness was substantially greater in the SHR-SP control group rats.


CONCLUSIONS
The study provides evidence that the diuretic compound indapamide improved the survival of SRH-SP even though their blood pressure was higher than that of untreated animals, and that genetic sensitivity to sodium, rather than blood pressure, influences the changes in arterial structure.
Levy
B I
BI
INSERM (U 141), Lariboisière Hospital, Paris, France.
Poitevin
P
P
Duriez
M
M
Guez
D C
DC
Schiavi
P D
PD
Safar
M E
ME
D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D001835:Body Weight / Q000187:drug effects / Q000502:physiology; D017536:Carotid Artery, Common / Q000187:drug effects* / Q000503:physiopathology*; D002561:Cerebrovascular Disorders / Q000235:genetics*; D003094:Collagen / Q000378:metabolism; D004232:Diuretics / Q000627:therapeutic use; D020022:Genetic Predisposition to Disease; D006973:Hypertension / Q000188:drug therapy / Q000235:genetics* / Q000503:physiopathology*; D007190:Indapamide / Q000627:therapeutic use; D008297:Male; D051381:Rats; D011918:Rats, Inbred SHR / Q000235:genetics; D012964:Sodium / Q000494:pharmacology*; D016019:Survival Analysis; D014666:Vasomotor System / Q000503:physiopathology
D004232:Diuretics; D003094:Collagen; D012964:Sodium; D007190:Indapamide